An uncommon site for a common crystal: Suspected popliteus tendon hydroxyapatite deposition disease.

Toyoda, T.; Sharrack, S.; Gupta, H.; Mankia, K.

An uncommon site for a common crystal: Suspected popliteus tendon hydroxyapatite deposition disease.

All Authors

Toyoda, T.

Sharrack, S.

Gupta, H.

Mankia, K.

LTHT Author

Toyoda, Task
Mankia, Kulveer
Sharrack, Sana
Gupta, Harun

LTHT Department

Doctors' Rotation
Rheumatology
NIHR Leeds Biomedical Research Centre
Radiology
Musculoskeletal Radiology

Publication Date

2025

Item Type

Conference Abstract

Abstract

Introduction: Hydroxyapatite deposition disease (HADD) is a self-limiting crystal arthropathy characterised by peritendinous or periarticular calcium hydroxyapatite crystal deposition, causing inflammation, pain and reduced range of movement. HADD most commonly affects the glenohumeral joint, particularly the supraspinatus tendon and adjacent bursae. Clinical presentation often mimics more common musculoskeletal conditions such as trauma, inflammatory arthritis and other crystal arthropathies, posing diagnostic challenges. While plain radiographs can detect calcific deposits, advanced imaging such as MRI provides superior sensitivity for identifying crystals and associated oedema. We report an unusual case of HADD affecting the posterolateral corner of the knee, diagnosed by characteristic MRI findings. Case description: We present the case of a 57-year-old male, with a history of type 2 diabetes mellitus and joint hypermobility with multiple previous shoulder subluxations and dislocations. He presented to his GP with a two-year history of intermittent left knee discomfort. These episodes were random in onset with no clear provoking factors. At the time, examination revealed no joint effusion or synovitis, full range of movement and normal gait. The symptoms were attributed to osteoarthritis and conservative management with physiotherapy and simple analgesia was advised. Four weeks later, he re-presented with sudden onset severe posterolateral left knee pain with no preceding trauma, resulting in significant difficulty weight-bearing and extreme pain on flexion of the left knee. The patient, who is a hospital consultant, had taken over-the-counter ibuprofen and paracetamol. An urgent MRI was ordered by an orthopaedic colleague and referral to rheumatology was made. He was assessed in rheumatology clinic one week after onset, by which time his symptoms had significantly improved. He denied any morning stiffness, joint swelling or previous gout. There was no family history of crystal arthropathy or autoimmune disease. Clinical examination showed full range of movement in the knee, with no tenderness, effusion or synovitis. Laboratory tests revealed normal inflammatory markers, calcium and uric acid and anti-cyclic citrullinated peptide antibodies and rheumatoid factor were negative. The MRI scan showed extensive soft tissue oedema in the posterolateral corner, superficial to the popliteus and a moderate knee joint effusion. There were low signal changes posterior to the popliteus tendon, in the posterolateral aspect of the knee with adjoining oedema. Given the severity of his presentation, yet rapid improvement and characteristic MRI changes, a diagnosis of acute HADD around the popliteus tendon was made. The patient was advised to take a short course of etoricoxib 60 mg should the pain re-occur. Discussion(s): This case underscores several important considerations. Firstly, although HADD predominantly affects the shoulder, awareness of atypical sites such as the popliteus tendon will mitigate misdiagnosis. The differential diagnosis for acute posterolateral knee pain is wide and includes traumatic, inflammatory, infectious and neoplastic causes. Awareness of HAAD in the knee is limited by the rarity and scarcity of literature. In this case, urgent MRI provided a pivotal role in revealing low-signal calcifications with surrounding oedema, aiding in the diagnosis. One consideration is that, unlike other crystal arthropathies where synovial fluid sampling can be performed to confirm the diagnosis, this is not typically undertaken in HADD. Therefore, the diagnosis relies primarily on the clinical presentation and imaging. In this case, the characteristic MRI findings together with the clinical picture makes this a highly plausible diagnosis of HADD. Second, although the exact pathogenesis remains unclear, a biological hypothesis exists between joint hypermobility and HADD. In this patient, joint hypermobility may have predisposed to tendon microtrauma, leading to inflammation and local hydroxyapatite crystal formation. Furthermore, diabetes-induced metabolic alterations such as increase in oxidative stress and chronic low-grade inflammation has been speculated to increase deposition of hydroxyapatite crystals and is a recognised risk factor for HADD. Here, the self-limiting nature of HADD was demonstrated, reflecting the resorptive phase in the natural history of the disease, where crystals rupture into the peritendinous space triggering acute inflammation, which subsides spontaneously as granulation and scar tissue forms. Conservative management alone sufficed, consistent with the current recommendations to reserve invasive interventions for refractory cases. Key learning points: This case highlights that although HADD is a relatively rare form of crystal arthritis, joint pain in certain predisposed individuals should prompt rheumatologists to consider it as a potential cause of symptoms, especially when more common causes have already been ruled out. Specific learning points gained through this case include the following: * Atypical location: HADD can involve the popliteus tendon, and more generally the knee, a site that is less recognised to be involved than the shoulder. Clinicians should include HADD in the differential of acute knee pain, especially when atraumatic. * Imaging diagnosis: Imaging such as MRI should be considered for aiding the diagnosis of atypical presentations to identify crystal deposition and/or surrounding oedema and to help exclude other causes of the presentation. This may help prevent unnecessary and invasive surgical exploration. * Risk factors: Predisposing risk factors such as joint hypermobility, diabetes mellitus, thyroid disease and oestrogen disorders can induce cellular stress and trigger degenerative calcification. These should be recognised and specifically asked about by clinicians to help inform diagnosis. * Pathophysiology and natural history: Understanding the formative, resorptive and remodelling phases of HADD can help anticipate the clinical course and can provide reassurance to the patient about the self-limiting nature of the disease. * Conservative management: Short course of NSAIDs are sufficient in most cases to effectively manage acute flares and prevents unnecessary invasive interventions.